The intestinal microbiota constitutes a true “extracorporeal organ” with an important role for the body's intrinsic metabolism and various immune functions. This “organ” performs unique digestive functions that simply cannot be accomplished by the gastrointestinal (GI) tract of a germ-free animal. However, together the GI and the microbiota form a complex metabolic cross talk among bacterial species and the host.
Normally the intestinal mucus layer protects the epithelium from invasion, and colonization by pathogens, and serves as a matrix in which antimicrobial factors produced by the epithelium, together with strains of the normal gut microbiota, reside. This mucus layer constitutes a buffer zone that achieves luminal compartmentalization of the microbiota and establishes a communication line for an exchange of molecules through crosstalks between bacterial strains and the intestinal epithelium (Sansonetti, Mucosal Immunol, 2011, 4:8-14).
An increasing antibiotic use in human and animal medicine, today leads to a severe amplification of antibiotic resistant strains in the gut such as methicillin resistant Staphylococci (MRSA and MRSE), extended spectrum β-lactamase producing Enterobacteriaceae (ESBL), vancomycin-resistant Enterococcus spp (VRE), clarithromycin-resistant Helicobacter pylori, vancomycin-resistant Clostridum difficile (CD), quinolone resistant Campylobacter jejuni and various strains of Candida species
CD is in small quantities part of the indigenous normal gut flora, but broad spectrum antibiotics such as clindamycin, cephalosporins, and fluoroquinolones, which destroy the indigenous human gut microflora, will cause gut overgrowth of CD which produces toxins, killing enterocytes in the mucosa, and induce diarrhea, which in severe cases leads to pseudomembranous colitis with a high mortality. The epidemic CD strain NAP1/027 produces substantially more toxin A and toxin B than hitherto isolated hospital strains and is highly virulent.
The gut microbiota is a complex ecosystem acting in symbiosis with the host. Enteric Bifidobacteria (Bif) species possess a very high number of genes to metabolise carbohydrates in the colon whereas lactobacilli are the dominating Lactic acid bacteria (LAB) in the small intestine.
Prebiotic fermentation produces short chain fatty acids (SCFA), such as acetic acid, butyric acid and lactic acid that reduce the local pH of the colon. Moreover, prebiotics and dietary fibers help in the multiplication of LAB and bifidobacteria to yield high cell densities and prevent growth of said gut pathogens mentioned above by producing bactericidal substances, antioxidants, reducing mucosal inflammation, maintaining colonic mucosal integrity, and promoting strong host anti-inflammatory responses. Competitive exclusion is another mode of antimicrobial defense against the invading pathogens.
The current use of the probiotic and prebiotic terms are normally related to a complementary synbiotic concept, wherein the probiotic is selected based on specific beneficial effects desirable for the host, and the prebiotic is selected to stimulate the growth of indigenous microflora. However, the present invention uses the approach of a novel synergistic concept, wherein the prebiotic is selected to stimulate the growth of probiotic strains having specific beneficial effects on the host. It may also increase the levels of beneficial host GI microbiota, but the primary target is to stimulate the growth of the ingested probiotic strains. Co-culturing stimulates other partners in the composition that are poor to utilize prebiotic oligosaccharides and other non-digestible carbohydrates in the human gut.